Special Topic

The Science and Theory behind Facial Aging

Jordan P. Farkas, MD
Joel E. Pessa, MD Summary: The etiology of age-related facial changes has many layers. Multi-
Bradley Hubbard, MD ple theories have been presented over the past 50–100 years with an evolution
Rod J. Rohrich, MD of understanding regarding facial changes related to skin, soft tissue, muscle,
and bone. This special topic will provide an overview of the current litera-
ture and evidence and theories of facial changes of the skeleton, soft tissues,
and skin over time. (PRS GO 2013;1:e8; doi:10.1097/GOX.0b013e31828ed1da;
Published online 5 April 2013.)
Downloaded from https://journals.lww.com/prsgo by BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3IOi9dz/r5OGv08t/C25emlxAbeN0cf8uM/CZuBTIfNaWh+yQ35cohw== on 05/26/2018

INTRODUCTION
The etiology of age-related facial changes has many
layers. Multiple theories have been presented over the
past 50–100 years with an evolution of understanding
regarding facial changes related to skin, soft tissue,
muscle, and bone.1–10 Historically, facial dystrophic
changes were attributed to gravity on the soft tissues
over time and the descent of the facial bony scaffold-
ing.11–14 Gonzalez-Ulloa and Flores15 presented their
theory on facial aging and “senility of the face” almost
50 years ago. They first described facial aging in rela-
tion to changes of the skin, descent of the soft tissues,
attrition of the facial septa, and craniofacial resorption
based on observation. Plastic surgeons have searched
to uncover the true myths behind facial aging in their
quest to restore attractive, youthful facial characteris-
tics in their patients. External environmental factors
such as body mass index, hormones, alcohol consump-
tion, cigarette smoking, and unprotected sun exposure
have all been associated with contributing to an accel-
erated appearance of facial aging.1 Pessa and Rohrich
et al6,15–26 have spent 3 decades in evaluating and
studying the anatomical facial changes that occur in
the facial skeleton and overlying soft tissues over time.
Earlier dogma of facial aging has only been recently
supplanted after careful adiographical and scientific
evidence of the tangible changes to facial skeleton,
soft tissue, and skin and the three-dimensionality of
From the Department of Plastic Surgery, University of Texas
Southwestern Medical Center, Dallas, Tex.
Copyright © 2013 American Society of Plastic Surgeons.
Unauthorized reproduction of this article is prohibited.
This is an open-access article distributed under the terms
of the Creative Commons Attribution-NonCommercial-
NoDerivatives 3.0 License, where it is permissible to download
and share the work provided it is properly cited. The work
cannot be changed in any way or used commercially.
DOI: 10.1097/GOX.0b013e31828ed1da
facial changes with time. This special topic will provide
an overview of the current literature and evidence and
theories of facial changes of the skeleton, soft tissues,
and skin over time.
FACIAL SKELETON
Original theories behind facial aging have
focused on soft-tissue laxity, ptosis, and descent
of the envelope over time on account of gravity.
Anatomical observational studies evaluating skeletal
morphological changes of the midface, mandible,
and orbit over time by authors such as Hellman,
Lambros et al, Pessa et al, and Shaw and Langstein et
al confirm bony facial remodeling over the course of
one’s life.7,20,25,27,28 Hellman7 identified that facial shape
continued to change throughout life and outlined
morphological differentiation of the facial skeleton.
Three-dimensional stereolithography and facial
computer topographic scanning provided radiological
evidence of the facial remodeling in young and old,
looking at specific changes to the maxilla, mandible,
pyriform, glabella, and orbits.20,21,25,28 Lambros and
Pessa et al uncovered the clockwise rotation of the
midface in relation to the cranial base in separate
younger and older individuals (Fig. 1). These studies
highlighted the characteristic changes in the aging
facial skeleton, concentrating on the posterior
displacement of the maxilla, lateral inferior shifting of
the lateral and inferior orbital rim, creating a larger
orbital aperture, and shrinking of the mandible in a
vertical and a horizontal plane. Pessa et al23 further
expanded on Hellman’s work confirming facial
skeletal “differentiation” with time, showing an
increase in mandibular size and shape over time and
Disclosure: The authors have no financial interest
to declare in relation to the content of this article. The
Article Processing Charge was paid for by the authors.

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Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.

Fig. 1. Age-related retrusion of the inferior orbital rim.
Reprinted with permission from Plast Reconstr Surg.
2000;106:479–488.
the sexual dimorphism in lower facial shape (Fig. 2).
These skeletal changes create dramatic shifting of
the overlying soft tissue and retaining ligaments of
the face, and when combined with fat atrophy and
Fig. 2. Age-related enlargement of the orbital aperture.
Reprinted with permission from Plast Reconstr Surg. 2000;
106:479–488.
2
Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
PRS GO • 2013
volume loss, these provide a tangible explanation
behind the complex, multifaceted etiology of facial
aging. Obviously, limitations to these studies are use
of different younger and older individuals in their
comparison; however, their findings should not be
dismissed. These landmark studies opened new doors
in understanding the complexities of facial aging
and the pivotal role of facial bony resorption and
remodeling. Changes to the bony scaffolding with time
inarguably lead to significant facial change and act in
concert with soft-tissue atrophy and laxity, creating the
appearance of aging.
A graduated level of understanding of these chang-
es leads to the development of specific treatment mo-
dalities designed to address the bony attrition with
techniques such as focused midface and chin implan-
tation and subperiosteally placed calcium hydroxyapa-
tite filler (ie, Radiesse).
FACIAL SOFT TISSUE AND FAT
COMPARTMENTS
The recent description of the superficial and
deep fat compartments of the face by Rohrich
and Pessa20 and radiological confirmation by
Gierloff et al29 not only reinforced the soft-tissue
compartmentalization of the face but also provided
further support of the theory of facial deflation and
volume changes to these compartments over time
(Figs. 3 and 4). Defined anatomical boundaries of
the nasolabial, medial, middle, lateral superficial
cheek, deep medial cheek, suborbicularis, buccal, and
periorbital fat compartments provide evidence of the
compartmentalization of the facial soft issues. Further,
injection studies performed by Pessa, Rohrich, and
Ristow et al highlighted the powerful topographical
changes that occur with limited volumetric changes
Fig. 3. The deep midfacial fat compartments. The deep
medial cheek fat is composed of a medial part (DMC) and a
lateral part (not shown). The medial part extends medially al-
most to the lateral incisor tooth. Augmentation of the deep
medial cheek fat will consequently elevate and efface the
nasolabial fold. The sub–orbicularis oculi fat is composed of
a medial part (MS) and a lateral part (LS). With aging, an infe-
rior migration occurs. Reprinted with permission from Plast
Reconstr Surg. 2012;129(1):263–273.
Farkas et al. • Theory behind Facial Aging
Fig. 4. Stylistic drawing of the facial fat compartments and
their aging changes. Aging leads to an inferior migration of
the midfacial fat compartments and an inferior volume shift
within the compartments. A deflation of the buccal exten-
sion of the buccal fat aggravates the inferior migration of
the medial cheek fat, middle cheek fat, and sub–orbicularis
oculi fat. Reprinted with permission from Plast Reconstr Surg.
2012;129(1):263–273.
Fig. 5. The knowledge of fat compartments enables a more
precise definition of facial anatomy. The malar fat, a term in-
troduced by Owsley, is composed of nasolabial fat, superior
medial fat, and the inferior infraorbital fat compartments.
These lie above superficial fascia and are therefore superfi-
cial fat compartments. Midfacial adipose tissue includes both
malar fat and the three deep periorbital fat compartments
described. Adapted from Plast Reconstr Surg. 2007;119:
2219–2227.
Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
Fig. 6. An artist’s rendition of the subcutaneous com-
partments of the face. Adapted from Plast Reconstr Surg.
2007;119:2219–2227.
in these specific areas of the face (Figs. 5 and 6).26
Attenuation of the zygomatic-cutaneous, orbitomalar,
and mandibular retaining ligaments of the face gives
the appearance of descent of the facial soft tissue,
and as anatomical studies have confirmed, it acts as a
hammock to the atrophied fat compartments and soft
tissues of the face, contributing to the morphological
appearance of the tear trough deformity, malar
bags, and jowling.5,6,11,12,17,29–33 The deflation and
loss of the normal anatomic subcutaneous facial fat
compartments gives off the appearance of increased
skin laxity or prominent folds around the nasolabial
region, periorbital region, and jowl.15–19,32–42 It was
once thought that along with atrophy and changes
of the facial fat over time, the mimetic musculature
and periosteum of the face also underwent similar
changes. However, using magnetic resonance imaging,
Gosain et al26 found that although facial soft tissues
underwent ptosis and subcutaneous hypertrophy in
the deep cheek over time, the mimetic musculature
was unchanged in volume and length.
The uncovering of fat compartmentalization of
the face has revolutionized the approach to facial
rejuvenation. Focused localized fat injection and/or
soft-tissue filler into discrete compartments, such as
the deep medial, and middle fat pads of the cheek,
has a dramatic effect on facial volume and reshaping
the soft tissues of the face into an anatomically more
youthful position.15–18 Fat injection techniques in
3

combination with the resuspension of the facial and
neck soft tissues through rhytidectomy, release of
the retaining ligaments, and/or superficial musculo-
aponeurotic system and platysma repositioning address
specific soft-tissue changes on an individualized basis.
Increasing anatomical understanding of facial soft-
tissue morphological changes over time allows for
tailoring of the rejuvenation techniques to specific
deficiencies uncovered with detailed facial analysis.
FACIAL SKIN
The skin is the envelope or canvas of the face,
revealing the deflation and atrophic changes of the
underlying bone and soft-tissue compartments as pre-
viously discussed. However, in addition, the skin also
goes through intrinsic changes over time on account
of external and internal factors.43,44 Some suggest that
repetitive dynamic muscle contractions result in the
appearance of superficial and deep rhytids over areas
of habitual muscle contractions such as the orbicular-
is oculi and oris, risorius, frontalis, and corrugators
on account of fascial partitioning and connections
of the dermis and periosteum between the different
facial muscle groups. Smoking and photodamage re-
sult in increased production of intracellular reactive
oxidative intermediates and species and cause a mul-
titude of facial skin changes resulting in epidermal
thinning, solar elastosis, and dermal collagen disor-
ganization, leading to characteristics consistent with
aging skin (Fig. 7).1,43,45,46
Solar elastosis is the term used to describe the his-
tologic appearance of the photoaged dermal extra-
cellular matrix. This condition is characterized by an
accumulation of amorphous, abnormal elastin mate-
rial surrounding a decreased volume and disorganized
array of wavy collagen fibrils.47–50 It is hypothesized that
the abnormal elastin results from overproduction of
normal elastin, which is subsequently degraded by the
chronic inflammatory state.47 The other major compo-
nents of extracellular matrix, glycoproteins and glycos-
aminoglycans (GAGs), tend to diminish with age, but
they are ironically increased in photoaged skin.43–46,49–53
Ultra violet A (UVA) and ultra violet B (UVB)
radiation causes direct and indirect damage to
skin through absorption of the Ultra violet (UV)
energy. The two most significant UV spectrum
chromophores in skin are DNA and urocanic acid.
Although UVA has been shown to directly induce
DNA changes, its main route of cell damage is indi-
rect, that is, through the creation of reactive oxygen
species and free radicals.46–55 Several matrix metal-
loproteinases combine to degrade the collagen
extracellular framework, leading to an increase in
oxidative stresses contributing to the degradation
of the surrounding collagen and increased elastin
4
Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
PRS GO • 2013
production. The epidermis undergoes characteristic
histological changes with sun damage, leading to in-
creased thickness, slower keratinocyte turnover, and
decreased melanocyte counts. However, there are
also regions of increased melanocyte concentration,
with increased capacity for melanin production and
deposition to keratinocytes, which present as solar
lentigines.46,54–58
It is important to remember that UVB light is
almost completely absorbed by the epidermis, and
thus dermal photodamage is solely caused by UVA.
In unprotected skin, there is an increase in all cells
and extracellular matrix contents, elastin, and GAGs,
and in fibroblast and Langerhans cells.48–51 UV radia-
tion has also been shown to increase angiogenesis
and likely accounts for the telangiectases seen in
sun-exposed skin.
In contrast to the epidermis, the histologic
picture of photoaged dermis on the cellular level
is one of chronic inflammation. Fibroblast and
Langerhans cells are decreased and surrounded by
abundant inflammatory infiltrate. Fibroblasts are
morphologically abnormal and produce less colla-
gen due to impaired signaling (lessened response to
transforming growth factor beta). Langerhans cells
decrease in number and undergo functional and
morphologic changes. Interestingly, other major
components of extracellular matrix, glycoproteins
and GAGs, tend to diminish with age, but they are
increased in photoaged skin.44–59 However, the in-
creased GAGs are not found in the papillary dermis
as usual; instead they are deposited in the reticular
dermis within the elastotic material and are not able
to regulate dermal hydration, leading to dry and
leathery-appearing skin.
There is unquestionably a powerful genetic com-
ponent to facial skin aging, which in turn plays a sig-
nificant role in overall skin appearance over time.
This is likely the most powerful intrinsic factor of the
appearance of skin aging.44–59
Of all topical treatment modalities and gimmicks
for skin wrinkle improvement and rejuvenation,
there is substantial level 1 evidence behind the
success of tretinoin in the treatment of photoaged
and damaged skin. Actions of tretinoin, which is
the active form of retinol, include prevention of the
activation of matrix metalloproteinases and oxidative
stress, and stimulation of regeneration of the ever-
important extracellular matrix. Retinoids also inhibit
keratinocyte differentiation and stimulate epidermal
hyperplasia with increased keratinocyte turnover
(Fig. 8). The addition of retinoids with various
resurfacing procedures has proven to be impressively
beneficial in the improvement of mild-to-moderate
facial rhytids.43,47–52,60–62
Farkas et al. • Theory behind Facial Aging

Fig. 7. Twins (natural age 61) with significant difference in sun exposure. Twin B (B)
had approximately 10 hours per week greater sun exposure than twin A (A). Twin
A had a body mass index 2.7 points higher than that of twin B. The perceived age
difference was 11.25 years. Reprinted with permission from Plast Reconstr Surg.
2009;123(4):1321–1331.

CONCLUSIONS tangible evidence have provided a foundation for

To adequately restore youthful facial characteristics, understanding the changes to the facial skin, soft
adequate understanding of facial morphological tissue, and bony scaffolding that have been theorized
changes over time in its entirety is essential. Over to contribute to facial aging. However, understanding
the past 20–30 years, sound scientific data and of facial changes over time is still in its infancy, and

5
Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.

Fig. 8. Before and after treatment (12 weeks) with 0.05% tret-
inoin. Increases in thickness of viable epidermis and decrease
in melanin pigment typically occur. Reprinted with permis-
sion from Plast Reconstr Surg. 1998;102(5):1667–1671.
facial changes can only truly be understood when
comparing the changes of the facial components in
a single individual at variable time points over the
course of a life as first instituted almost a century
ago with the Bolton-Brush longitudinal growth
study at Case Western Reserve School of Dentistry.7,23
Obviously, the evaluation of radiographical and/or
anatomical changes of the same person over time is
quite difficult. However, the historical theories of facial
aging being attributed to the descent of soft tissues
have now not only been validated by sound anatomical
and radiographical observational studies but also
expanded on advancing our understanding of the
complexities of overall facial morphological change
with time.8–10 The recent uncovering of anatomical
facial fat compartment anatomy has revolutionized
the concept and approach of adding volume to
specific deflated soft-tissue compartments, creating a
more individualized youthful restoration to the face.
The outstanding improvement in understanding has
compartmentalized the treatment strategy to facial
rejuvenation. Restoring youthful characteristics starts
from the skeletal framework and builds progressively to
the canvas of the face. With proper diagnosis and facial
6
Copyright © 2013 American Society of Plastic Surgeons. Unauthorized reproduction of this article is prohibited.
PRS GO • 2013
analysis, specific age-related changes can be addressed.
By improving the skeletal proportions of the midface
with calcium hydroxyapatite, or implants, or restoring
proper position and volume of the soft tissues with fat
grafting and manipulation of the superficial musculo-
aponeurotic system and lid structures, or lastly through
skin rejuvenation with tretinoin, botulinum injections,
or resurfacing, youthful characteristics of the face can
be restored in a stepwise organized fashion that is
tailored to the specific changes in the individual.
Morphological changes to the facial skeletal frame-
work, soft tissue, retaining ligaments, fat compart-
ments, and skin envelope all contribute to facial aging
in variable degrees depending on the intrinsic and
extrinsic factors highlighted in this report. To provide
our patients with the best possible rejuvenation strate-
gy, appropriate diagnosis of the physiological changes
of each of the elements of facial aging is imperative.
Jordan P. Farkas
Department of Plastic Surgery
University of Texas Southwestern Medical Center
Dallas, TX 75390-9132
E-mail: jpfarkasmd@gmail.com.
PATIENT CONSENT
Patients provided written consent for the use of their
images.
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